Englund 2022 Mol Metab

From Bioblast
Publications in the MiPMap
Englund DA, Jolliffe A, Aversa Z, Zhang X, Sturmlechner I, Sakamoto AE, Zeidler JD, Warner GM, McNinch C, White TA, Chini EN, Baker DJ, van Deursen JM, LeBrasseur NK (2022) p21 induces a senescence program and skeletal muscle dysfunction. https://doi.org/10.1016/j.molmet.2022.101652

Β» Mol Metab 67:101652. PMID: 36509362 Open Access

Englund Davis A,  Jolliffe Alyssa,  Aversa Zaira,  Zhang Xu,  Sturmlechner Ines,  Sakamoto Ayumi E,  Zeidler Julianna D,  Warner Gina M,  McNinch Colton,  White Thomas A,  Chini Eduardo N,  Baker Darren J,  van Deursen Jan M,  LeBrasseur Nathan K (2022) Mol Metab

Abstract: Recent work has established associations between elevated p21, the accumulation of senescent cells, and skeletal muscle dysfunction in mice and humans. Using a mouse model of p21 overexpression (p21OE), we examined if p21 mechanistically contributes to cellular senescence and pathological features in skeletal muscle. We show that p21 induces several core properties of cellular senescence in skeletal muscle, including an altered transcriptome, DNA damage, mitochondrial dysfunction, and the senescence-associated secretory phenotype (SASP). Furthermore, p21OE mice exhibit manifestations of skeletal muscle pathology, such as atrophy, fibrosis, and impaired physical function when compared to age-matched controls. These findings suggest p21 alone is sufficient to drive a cellular senescence program and reveal a novel source of skeletal muscle loss and dysfunction. β€’ Keywords: Cellular senescence, DNA damage, Aging, Fibrosis, Physical function, Sarcopenia, Senescence-associated secretory phenotype β€’ Bioblast editor: Plangger M

Labels: MiParea: Respiration, Genetic knockout;overexpression  Pathology: Aging;senescence 

Organism: Mouse  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 

Coupling state: LEAK, OXPHOS, ET  Pathway: N, S, NS, ROX  HRR: Oxygraph-2k 


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